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Caspase-3 and prostaglandins signal for tumor regrowth in cancer therapy

Abstract

Chemo- and radio-therapeutic regimens frequently kill cancer cells by inducing apoptosis, a cell-death subroutine that involves the activation of a particular class of proteases called caspases. In a recent issue of Nature Medicine, Huang et al. (2011) show that caspase activation in dying tumor cells causes the release of soluble lipid messengers, notably prostaglandin E2, that stimulate tumor cell proliferation. In this short review, we will discuss the clinical and therapeutic implications of these findings.

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Figure 1

Abbreviations

iPLA2:

cytosolic Ca2+-independent phospholipase A2

PGE2:

prostaglandin E2

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Acknowledgements

The authors are supported by the Ligue contre le Cancer (équipe labellisée, AXA Chair for Longevity Research, Cancéropôle Ile-de-France, Institut National du Cancer (INCa), Fondation Bettencourt-Schueller, Fondation de France, Fondation pour la Recherche Médicale, Association Laurette Fugain, Cent pour Sang la Vie, Agence National de la Recherche, FRM and the European Commission (Apo-Sys, ArtForce, ChemoRes. Death-Train) and the LabEx Immuno-Oncology.

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Correspondence to G Kroemer.

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Galluzzi, L., Kepp, O. & Kroemer, G. Caspase-3 and prostaglandins signal for tumor regrowth in cancer therapy. Oncogene 31, 2805–2808 (2012). https://doi.org/10.1038/onc.2011.459

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